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MYOD represses gene expression from non-Ebox motifs

GSE283209 Mus musculus (mouse) ChIP-seq / ATAC-seq (genome binding and open chromatin) 98 samples Submitted 2025/08/08 Platform GPL34281Platform GPL34475Platform GPL34328
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · mouse · 98 samples

What it is
ChIP-seq / ATAC-seq (genome binding and open chromatin)Where proteins bind the genome, or which regions are open and active.
Organism
Mus musculus (mouse)
Samples
98 samples: 39 conditions, mostly in duplicateGroups are read from the sample names, not from the paper. Check the list below.
Data you can get
A processed table (series matrix) and supplementary files from NCBI; the raw sequencing reads from ENA. Which of these hold counts depends on the study, so check the file list.
Paper
MYOD represses gene expression from non-E-box motifsGenes & development · 2025
Summary (written by the submitters)
We report on the identification of a previously unrecognized property of MYOD as repressor of gene expression, via E-box-independent chromatin binding, during the process of somatic cell trans-differentiation into skeletal muscle. When ectopically expressed in proliferating human fibroblasts or endogenously induced in activated muscle stem cells (MuSCs) MYOD was detected at accessible regulatory elements of expressed genes, invariably leading to reduced chromatin accessibility and gene repression.
Read the full summary ↓
At variance with conventional E-box-driven increased chromatin accessibility and H3K27 acetylation at previously silent loci of MYOD-activated genes, MYOD-mediated chromatin compaction and repression of transcription was associated with high occurrence of non-E-box motifs, did not lead to reduced levels of H3K27ac and coincided with reduced levels of H4 acetyl-methyl lysine modification (Kacme). Using MYOD mutants we dissected the molecular mechanism of MYOD-mediated repression, whereby repression of mitogen- and growth factor-responsive genes occurred via promoter binding, which requires a conserved domain within the first helix; conversely, repression of cell-of-origin/alternative lineage genes occurred via binding and decommissioning of distal regulatory elements, such as super-enhancers (SE), it required either the N-terminal activation domain or the two chromatin-remodeling domains, and it coincided with reduced strength of CTCF-mediated chromatin interactions. These data extend MYOD biological properties beyond the current dogma that restricts MYOD function to a monotone transcriptional activator. They also reveal an unprecedented functional versatility arising from alternative chromatin recruitment through E-box or non-E-box sequences, whereby genetic determinants dictate differential usage of MYOD functional domains.
Published in
MYOD represses gene expression from non-E-box motifs
Nicoletti C, Massenet J, Pintado-Urbanc AP et al. · Genes & development 2025 · PMID 40769720 · doi:10.1101/gad.352708.125
This dataset
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Download · which file do I need?

Direct links to NCBI and ENA, no account and no request form. Pick by what you want to do: take the small processed table to look, the supplementary files to re-analyse, or the original raw data to start over.

1 · Just have a look

Processed table

The series matrix: one table of values per sample as the submitters processed it. The smallest download, and it opens in Excel or R. Start here to see what the data look like.

Series matrix ↓
2 · Re-analyse it

Supplementary files

The count tables and other files the authors uploaded. Take only the samples you need, or the whole study as GSE283209_RAW.tar (it can run to tens of gigabytes).

All supplementary files ↗ Whole study · RAW.tar ↓
3 · Start from the raw reads

Raw sequencing reads

The original FASTQ files, straight from the sequencer, held at ENA. Large, and you align them yourself, so only choose this if you need to re-process the study from scratch.

Raw reads on ENA ↗

What the files usually look like: Look for peak files (.bed, .narrowPeak) and signal tracks (.bigWig) among the supplementary files; the raw reads are on ENA.

Also filed as BioProject PRJNA1192514 and SRA study SRP548521. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 40769720) ↗
Study design
39 conditions, mostly in duplicate
RNAseq, IMR90, Empty vector, ×3 RNAseq, IMR90, MyoD WT vector, ×3 RNAseq, IMR90, MyoD D102-114 vector, ×3 RNAseq, IMR90, MyoD D102-135 vector, ×3 ATACseq, IMR90, MyoD D102-114 vector, ×3 ATACseq, IMR90, MyoD D102-135 vector, ×3 ATACseq, IMR90, Empty vector, ×3 ATACseq, IMR90, MyoD WT vector, ×3 +41 more

Supports a between-group comparison across 88 samples.

How we read this: 39 replicated groups read from 98 sample titles; they account for 88 of them. These groups are guessed from the sample names, not taken from the paper, so check them against the sample list below before relying on them.

Samples in this study

+ 58 more — browse all 98 samples with per-sample file links →

Datasets on a similar topic

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